Electron Microscope Studies of Experimental Entamoeba Histolytica Infection in the Guinea Pig

Takeuchi, Akio; Phillips, Bruce P.

doi:10.4269/ajtmh.1975.24.34

Cited by 96 publications

(62 citation statements)

References 23 publications

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“…Furthermore, once inside the host cell, S.¯exneri lyses the membrane-bound phagocytic vacuole, grows within the cytoplasmic compartment and promotes intercellular spreading using the host cytoskeleton as a motor (Makino et al, 1986;Bernardini et al, 1989;Goldberg and Sansonetti, 1993). Conversely, S. typhimurium remain in their membrane-bound vacuole as they transit across the intestinal epithelium, where they are ultimately deposited in the lamina propria in order to make their way into the reticuloendothelial system (Takeuchi, 1967;Day et al, 1978;McGovern and Slavutin, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Invasion of certain bacterial pathogens, including S. typhimurium and Shigella¯exneri, into the intestinal epithelium is accompanied by transepithelial migration of PMNs in the basolateral-to-apical direction. Such transmigration of PMNs across intestinal epithelia leads to a disease state of acute intestinal in¯ammation and is a hallmark of bacterial enterocolitis caused by S. typhimurium (Takeuchi, 1967;Rout et al, 1974;Day et al, 1978;McGovern and Slavutin, 1979;Kumar et al, 1982) and Shigella spp. (Mathan and Mathan, 1986;Bennish, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

et al. 1999

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SummaryDysentery caused by Shigella species is characterized by in®ltration of polymorphonuclear leucocytes (PMNs) into the colonic mucosa. Shigella spp. evolved into pathogens by the acquisition of virulence genes and by the deletion of`antivirulence' genes detrimental to its pathogenic lifestyle. An example is cadA (encoding lysine decarboxylase), which is uniformly absent in Shigella spp., whereas it is present in nearly all isolates of the closely related non-pathogen Escherichia coli. Here, using monolayers of T84 cells to model the human intestinal epithelium, we determined that the introduction of cadA into S.¯exneri and the expression of lysine decarboxylase attenuated the bacteria's ability to induce PMN in¯ux across model intestinal epithelium. Such inhibition was caused by cadaverine generated from the decarboxylation of lysine. Cadaverine treatment of model intestinal epithelia speci®cally inhibited S.¯exneri induction of PMN transepithelial migration, while having no effect on the ability of Salmonella or enteropathogenic E. coli (EPEC) to induce PMN migration. These observations not only provide insight into mechanisms of S.¯exneri pathogen evolution and pathogenesis, but also suggest a potential for the use of cadaverine in the treatment of dysentery.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

et al. 1999

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“…The histopathologic hallmark of human Salmonellosis, caused by non-typhoidal strains of Salmonella enterica of which S. typhimurium is one of the most common serovars, is the recruitment of neutrophils to the intestinal mucosa resulting in the formation of an intestinal crypt abscess (Takeuchi, 1967).…”

Section: Discussionmentioning

confidence: 99%

Salmonella typhimuriumtranscytoses flagellin via an SPI2-mediated vesicular transport pathway

Lyons

Wang

Casanova

et al. 2004

Journal of Cell Science

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Apical colonization of polarized epithelia by Salmonella typhimurium results in translocation of flagellin to the basolateral membrane domain, thus enabling activation of toll-like receptor 5 (TLR5)-mediated pro-inflammatory gene expression. Such flagellin transcytosis occurred without a change in epithelial permeability to 40 kDa FITC dextran, did not require bacterial motility and was independent of transepithelial movement of intact bacteria. Flagellin transcytosis was blocked at 20°C, suggesting dependence on vesicular transport consistent with results from confocal microscopy that showed flagellin independent of bacteria inside epithelial cells. Furthermore, vesicles isolated from S. typhimurium-infected epithelia were highly enriched in flagellin. Flagellin transcytosis was dependent upon genes of Salmonella pathogenicity island (SPI)-2, which alter vesicular trafficking, but independent of SPI-1 that mediates bacterial invasion. Furthermore, such SPI-2 mutants were unable to mediate the localization of flagellin into intracellular vesicles consistent with flagellin transcytosis mediated by a S. typhimurium take-over of host vesicle trafficking pathways. As a result of their inability to transcytose flagellin, apical colonization by SPI-2 mutants induced substantially less epithelial IL-8 secretion than wild-type strains suggesting that such SPI-2 mediated transcytosis of flagellin plays a role in the pathogenesis of the mucosal inflammation characteristic of human Salmonellosis.

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“…Takeuchi [1] described a two step process of association between salmonella with the gut epithelium prior to cellular (enterocyte) uptake and suggested that bacterial cell surface components, possibly fimbrial structures, may have initiated this association.…”

Section: Introductionmentioning

confidence: 99%

Distribution, gene sequence and expressionin vivoof the plasmid encoded fimbrial antigen ofSalmonellaserotype Enteritidis

1996

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SUMMARYThe pefA gene which encoded the serotype associated plasmid (SAP) screened by hybridization for the presence of pef sequences. Recombinant clones which were deduced to harbour the entire pef operon elaborated a PEF-like fimbrial structure at the cell surface. The PEF-like fimbrial antigen was purified from one cosmid clone and used in western blot experiments with sera from chickens infected with Enteritidis phage-type 4. Seroconversion to the fimbrial antigen was observed which indicated that the Enteritidis PEF-like fimbrial structure was expressed at some stage during infection. Nucleotide sequence analysis demonstrated that the pefA alleles of Typhimurium and Enteritidis phage-type 4 shared 76 % DNA nucleotide and 82 % deduced amino acid sequence identity.

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Electron Microscope Studies of Experimental Entamoeba Histolytica Infection in the Guinea Pig

Cited by 96 publications

References 23 publications

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

Inhibition of Shigella flexneri-induced transepithelial migration of polymorphonuclear leucocytes by cadaverine

Salmonella typhimuriumtranscytoses flagellin via an SPI2-mediated vesicular transport pathway

Distribution, gene sequence and expressionin vivoof the plasmid encoded fimbrial antigen ofSalmonellaserotype Enteritidis

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